“Pancreatic α-cells and glucagon—neglected metabolic actors”

When, in 1921, Banting and Best tested their first pancreatic extracts in depancreatized dogs, they noticed that a mild, but reproducible hyperglycemia preceded the hoped-for hypoglycemic effect. The phenomenon was attributed to the presence of a glucogenic substance in the pancreatic extracts by Murlin and colleagues in1923 who gave it the name “glucagon” or mobilizer of glucose. Roger Assan and his coworkers at the Hôtel Dieu (Paris) were the first to report extremely high circulating glucagon levels in ten patients with severe diabetes ketoacidosis and how these levels rapidly fell on treatment.1 The more universal character of the absolute or relative hyperglucagonemia of diabetes was established by Unger et al in 19712 (Lefebvre, Lecture). Nowadays, it is admitted that diabetes is manifested as insufficient release of the hypoglycemic hormone insulin combined with impaired regulation of glucagon secretion. The abnormalities of glucagon secretion are twofold: too much glucagon is secreted during hyperglycemia and too little is released during hypoglycemia (Rorsman, Lecture). During the XIIth symposium of the International Group on Insulin Secretion (IGIS), supported by an unrestricted educational grant from Servier, the foremost international specialists in the field of the α-cells, glucagon, and diabetes presented their most recent research findings. Below is a summary of the main points addressed.